Long-Term Persistence of the Urine Calcium-Lowering Effect of Potassium Bicarbonate in Postmenopausal Women
Frassetto L et al, Dept of Medicine and General Clinical Research, U of California, San Francisco, CA. Journal of Endocrinology & Metabolism 90(2):831-834, 2005
Age-related bone mass decline entails loss of bone calcium. Bone might lose calcium in part because its alkaline calcium salts titrate noncarbonic acids endogenously produced in response to habitual ingestion of the net acid-producing diets typical of Western countries. The acid-liberated bone calcium disappears in urine, proportionate to the magnitude of the diet net acid load. Although the kidney daily excretes the bulk of the diet net acid load, the body retains a small fraction sufficient to induce a persisting low-grade metabolic acidosis, which ensures continued titration of the alkaline salts of bone, with attendant loss of calcium and phosphorus in urine. The diet-induced low-grade metabolic acidosis that persists further contributes to the external losses of calcium by direct impairment of renal calcium reabsorptive efficiency, a characteristic of metabolic acidosis.
Potassium bicarbonate (KBC) potently reduces urine calcium excretion in adult humans, including patients with hypertension or calcium urolithiasis, and postmenopausal women, who have substantial risk of calcium deficiency. We studied 170 postmenopausal women randomized to KBC 30, 60, or 90 mmol/d (KBC treatment), or placebo, for up to 36 months. Each received a multivitamin with 400 IU vitamin D, and calcium carbonate as needed to produce a total dietary calcium intake of at least 30 mmol daily.
Daily urine calcium excretion (UcaV) did not differ among groups at baseline. From 1-36 months of KBC treatment, adjusting UcaV for creatinine (Cr) excretion, each dose of KBC reduced UcaV with a dose-dependent trend. The reduced UcaV/Cr persisted throughout the KBC treatment period (up to 36 months) in all KBC, and the greatest reductions occurred in the subjects with greatest baseline UcaV/Cr.
28% of the subjects had high baseline calciuria (UcaV/Cr > 200 mg CA/1000 mg Cr). With baseline UcaV/Cr of 250 mg/1000 mg Cr, KBC 60 mmol decreased UcaV/Cr by 55.8 mg/1000 mg Cr, a potential daily calcium retention that over a 36-month period would accumulate up to 55,845 mg of calcium, nearly 5% of bone calcium content.
KBC treatment induced a dose-dependent decrease in UcaV/Cr that persisted up to 36 months, with the greatest decreases occurring in those women with the greatest baseline UcaV, nearly a third of whom had high baseline calciuria. Thus, one can preselect postmenopausal women most likely to have the urine calcium-lowering effect of KBC and predict their potential bone calcium increase.
This study demonstrates that in normal postmenopausal women eating a typical American diet, supplementing dietary potassium with potassium bicarbonate (potassium alkalizing salt) induces a reduction in urinary excretion of calcium that persists over a period of up to 36 months. More importantly, the women at the greatest risk for body calcium loss (ie. hypercalciuric subjects at baseline) had the greatest decline in urinary excretion of calcium and would potentially derive the greatest benefit from treatment with potassium bicarbonate, and potentially decrease the incidence of osteoporosis.
Supplementation with alkaline minerals reduces symptoms in patients with chronic low back pain.
Vormann J. et al., Institut fur Pravention und Ernahrung, Ismaning, Germany. J Trace Elem Biol 2001;15(2-3):179-83.
The cause of low back pain is heterogeneous, it has been hypothesised that a latent chronic acidosis might contribute to these symptoms. It was tested whether a supplementation with alkaline minerals would influence symptoms in patients with low back pain symptoms.
In an open prospective study 82 patients with chronic low back pain received daily 30 g of a lactose based alkaline multimineral supplement (Basica) over a period of 4 weeks in addition to their usual medication. Pain symptoms were quantified with the "Arhus low back pain rating scale" (ARS). Mean ARS dropped highly significant by 49% from 41 to 21 points after 4 weeks supplemention. In 76 out of 82 patients a reduction in ARS was achieved by the supplementation. Total blood buffering capacity was significantly increased from 77.69 +/- 6.79 to 80.16 +/- 5.24 mmol/L (mean +/- SEM, n = 82, p < 0.001) and also blood pH rose from 7.456 +/- 0.007 to 7.470 +/- 0.007 (mean +/- SEM, n = 75, p < 0.05). Only intracellular magnesium increased by 11% while other intracellular minerals were not significantly changed in sublingual tissue as measured with the EXA-test. Plasma concentrations of potassium, calcium, iron, copper, and zinc were within the normal range and not significantly influenced by the supplementation. Plasma magnesium was slightly reduced after the supplemenation (-3%, p < 0.05).
The results show that a disturbed acid-base balance may contribute to the symptoms of low back pain. The simple and safe addition of an alkaline multimineral preparate was able to reduce the pain symptoms in these patients with chronic low back pain.
Oral sodium bicarbonate for the treatment of metabolic acidosis in peritoneal dialysis patients: a randomized placebo-control trial.
Szeto CC et al., The Chinese University of Hong Kong, Shatin, Hong Kong. J Am Soc Nephrol 2003 Aug;14(8):2119-26.
Acidosis causes malnutrition in peritoneal dialysis (PD) patients. The effect of oral bicarbonate in PD patients with Kt/V <2.1 has not been studied.
We randomly assigned 60 PD patients with acidosis and Kt/V <2.1 to oral sodium bicarbonate (0.9 g thrice daily) or placebo. Patients were followed for 12 mo. We compared their nutritional status, including subjective global assessment (SGA) score and normalized protein nitrogen appearance (NPNA), hospitalization and all-cause mortality. Treatment with oral bicarbonate resulted in a higher plasma bicarbonate level at 4 wk (27.8 +/- 2.6 versus 24.7 +/- 3.9 mmol/L, P = 0.002), and the difference persisted until 52 wk. Bicarbonate treatment had a significant effect on the change in overall SGA score (repeated measures ANOVA, P = 0.0003). The overall SGA score of the treatment group was higher than the placebo group at 24 wk (5.07 +/- 0.94 versus 4.40 +/- 1.00, P = 0.015), and the difference persisted thereafter. NPNA rose in the treatment group (1.17 +/- 0.32 to 1.28 +/- 0.26 g/kg per d, P = 0.034), but declined in placebo group (1.13 +/- 0.25 to 1.03 +/- 0.28 g/kg per d, P = 0.054). The treatment group had a shorter hospitalization than the placebo group (8.4 +/- 17.7 versus 16.8 +/- 21.7 d/yr; P = 0.02). Mortality was not significantly different.
Although our trial has limited statistical power, we find that in PD patients with mild acidosis and Kt/V <2.1, oral sodium bicarbonate probably improve nutritional status and reduce the duration of hospitalization.
Direct effect of the correction of acidosis on plasma parathyroid hormone concentrations, calcium and phosphate in hemodialysis patients: a prospective study.
Movilli E et al., University of Brescia, Brescia, Italy. Nephron 2001 Mar;87(3):257-62
BACKGROUND: Metabolic acidosis contributes to renal osteodystrophy and together with hyperphosphatemia, hypocalcemia and altered vitamin D metabolism may result in increased levels of intact parathyroid hormone (iPTH) and metastatic calcifications. However, the impact of the correction of metabolic acidosis on iPTH levels and calcium-phosphate metabolism is still controversial.
STUDY DESIGN: The effects of the correction of metabolic acidosis on serum concentrations of iPTH, calcium (Ca), phosphate (PO(4)) and alkaline phosphatase were prospectively studied. Twelve uremic patients on maintenance hemodialysis (HD) for 49 months (median; range 6-243 months) with serum bicarbonate levels < or =20 mmol/l were studied before and after 3 months of oral sodium bicarbonate supplementation. Predialysis serum bicarbonate, arterial pH, ionized calcium, plasma sodium, plasma potassium, serum creatinine, hemoglobin, K(t)/V, postdialysis body weight, predialysis systolic and diastolic blood pressure were also evaluated before and after correction. RESULTS: Serum bicarbonate levels and arterial pH increased respectively from 19.3 +/- 0.6 to 24.4 +/- 1.2 mmol/l (p < 0.0001) and 7.34 +/- 0.03 to 7.40 +/- 0.02 (p < 0.001). iPTH levels decreased significantly from 399 +/- 475 to 305 +/- 353 pg/ml (p = 0.026). No changes in total serum Ca, plasma PO(4), serum akaline phosphatase, K(t)/V, serum creatinine, hemoglobin, body weight, predialysis systolic and diastolic blood pressures were observed. iCa decreased significantly.
CONCLUSIONS: Our study demonstrates that the correction of metabolic acidosis in chronic HD patients reduces iPTH concentrations in HD patients with secondary hyperparathyroidism possibly by a direct effect on iPTH secretion.